ArticleArchives of medical science : AMS2026
Propofol attenuates cerebral ischemia-reperfusion-mediated neuronal apoptosis and oxidative damage by regulating the miR-6838-5p/AQP11 axis.
Article in Archives of medical science : AMS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: This study aimed to elucidate the mechanism by which propofol (PPF) exerts its effects in cerebral ischemia-reperfusion injury (CI/RI). Material and methods: A rat model of CI/RI was established via middle cerebral artery occlusion/reperfusion (MCAO/R). MCAO/R rats were pre-treated with PPF (10 mg/kg) via intraperitoneal injection. Additionally, 48 h before PPF administration, miR-6838-5p agomir/antagomir and aquaporin-11 (AQP11) lentiviral overexpression vectors were injected into MCAO/R rats. Infarct size was determined using 2,3,5-triphenyl tetrazolium chloride staining. Neurological function was assessed using standardized scoring, and cerebral edema was measured by determining brain water content. Hematoxylin-eosin staining, Nissl staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining were performed on brain tissues. Inflammatory and oxidative markers were evaluated. A hypoxia/reoxygenation (H/R) injury model was established in PC12 cells to assess miR-6838-5p and AQP11 expression levels, as well as cell viability and apoptosis. Results: The lethal dose 50 (LD Conclusions: PPF ameliorates CI/RI by modulating the miR-6838-5p/AQP11 axis.
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